Today, thank you for standing by. Welcome to Tango Therapeutics' clinical data update conference call and webcast. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. Please note that today's conference may be recorded. I will now hand the conference over to your speaker host, Elizabeth Hickin of Investor Relations. Please go ahead. Thank you. Good morning, everyone, and thank you for joining today's call to discuss the vopimetostat clinical data. This morning, we issued a press release on the data, which can be found on the Investors and Media section of our website, www.tangotx.com. On today's call, Tango Therapeutics' President and Chief Executive Officer Dr. Barbara Weber and President of R&D Dr. Adam Crystal will walk us through the data. At the conclusion of prepared remarks, we will open the call to Q&A, and we'll be joined by CFO Daniella Beckmann. Before we begin, let me review our safe harbor statement. On today's call, we will be making forward-looking statements that reflect our beliefs as of today and are subject to risks and uncertainties as outlined in our filings with the SEC. I will turn it over to Dr. Barbara Weber. Thank you, Liz, and welcome, everyone. Today, we are pleased to provide a clinical update on TNG462, our lead PRMT5 inhibitor, now formally named vopimetostat. As brief background, we launched Tango in 2017 based on the idea that the genetic concept of synthetic lethality offered an opportunity to discover and develop cancer drugs targeting genes that are frequently deleted in human cancers and to contribute to building the arsenal of novel cancer drugs that have changed the lives of so many people with cancer over the past 20 years. vopimetostat is an example of such a drug, specifically designed to work in cancers with MTAP deletion, largely sparing normal cells. vopimetostat is an oral, once-daily PRMT5 inhibitor we are developing for multiple cancer types with MTAP deletion, one of the most common genetic alterations in human cancers, found in 10% to 15% of all solid tumors. Our initial development focus is on pancreatic cancer, with approximately 20,000 MTAP-deleted cases annually in the U.S. The data from our phase I/II study support plans for our first pivotal study, starting in 2026, in second-line MTAP-deleted pancreatic cancer, providing a path for vopimetostat to be the first MTAP-selective PRMT5 inhibitor to market. In considering plans for development in first-line pancreatic cancer, we believe that RAS inhibitors will change the treatment paradigm in the coming years. Thus, we started a trial last summer of vopimetostat in combination with the RAS-on inhibitors, daraxonrasib and zoldonrasib, in collaboration with Revolution Medicines. These combinations provide a potential path to a chemotherapy-free first-line treatment of MTAP-deleted pancreatic cancer, a tribute to our friend and colleague Dimitris Papoutsakis, who died of pancreatic cancer just before his 50th birthday in 2021, and just a little bit too soon to benefit from the remarkable progress now being made in this disease. MTAP-deleted lung cancer is another important development focus for us, representing approximately 22,000 patients in the U.S. annually. We anticipate a data update from the monotherapy cohort of our phase I/II trial as those data mature in 2026. Finally, the data we will review today provides the basis for developing vopimetostat in the 13 different cancer types represented in the histology-agnostic cohort of our study. This group of multiple difficult-to-treat cancer types accounts for another 20,000 MTAP-deleted cancers in the U.S. each year, bringing the total population of MTAP-deleted solid tumors to more than 60,000 patients per year in the U.S. As a reminder of the study design and to provide context for the data we will present today, the dose escalation cohort included any solid tumor with an MTAP deletion. For dose optimization, we enrolled patients in three cohorts: pancreatic cancer, lung cancer, and a group we are calling histology agnostic. Today, we will provide data from the study as a whole, as well as an analysis of the pancreatic and histology agnostic cohorts. While we have enrolled more than 40 patients in the lung cancer cohort, enrollment to this cohort has taken longer than the others due to the large number of competing lung cancer trials. These data are not yet sufficiently mature and will be presented in 2026. The details of our disclosure today are shown here. Following this update, we have a strong cadence of disclosures planned for 2026. These will include initial data from our ongoing combination of vopimetostat plus the RAS-on inhibitors from Revolution Medicines in second-line plus pancreatic and lung cancers, initial data from a planned cohort of first-line pancreatic cancer patients, along with a more fulsome update on the second-line plus cohorts, clinical data from the monotherapy lung cancer cohort as it matures, and initial data on TNG456 and MTAP-selective PRMT5 inhibitors similar to vopimetostat in potency and selectivity that is brain-penetrant. TNG456 is being developed in glioblastoma, another indication of high unmet need, representing approximately 7,000 MTAP-deleted patients per year in the U.S. Now, I would like to introduce Dr. Adam Crystal, our President of R&D, who will provide the data update. Thank you, Barbara. I'd like to begin by highlighting key data that underscore our strong conviction in vopimetostat as the potentially first-in-class and best-in-class PRMT5 inhibitor. The observed overall response rate is 27%, which compares favorably to published competitor data. The FDA has agreed with our selected go-forward dose of 250 mg and that we have satisfied the conditions of Project Optimus. In second-line pancreatic cancer patients, the median PFS is 7.2 months, and the overall response rate is 25%, more than double the historical standards of care supporting our planned pivotal study. In the histology-agnostic cohort of heavily pretreated, poor-prognosis cancers, the overall response rate is 49%, with a median PFS of 9.1 months. Finally, vopimetostat has the best-in-class safety profile and tolerability profile to date, with no drug-related discontinuations and a dose reduction rate of 8%. With vopimetostat, as with other PRMT5 inhibitors, overall response rate is a time-dependent variable. This effect is demonstrated here. When all evaluable patients are assessed for response, the overall response rate is 20%, and with additional follow-up, the overall response rate increases to 27%. For this reason, the overall response rate analyses presented today are derived from patients enrolled more than six months before the data cutoff, regardless of outcome, in order to avoid underreporting response rates. As noted, the overall response rate for vopimetostat across all histologies is 27%, currently best in class across published data sets. Notably, the majority of partial responses occur after the first scan, with the longest time to first response being eight months in a patient with lung cancer. There are several other key data points worth highlighting. The median PFS is 6.4 months, an increase of almost a month compared to our update in November 2024, when we reported a median PFS of 5.5 months. This demonstrates that durability also continues to improve with increasing follow-up. Finally, almost 40% of patients remain on study, remarkable with a median follow-up of 9.4 months in heavily pretreated patients enrolled in a phase I study. This spider plot of all evaluable patients treated at active doses further demonstrates the durability seen in patients with partial response and those with stable disease, even those with more modest tumor regression. While the median PFS is 6.4 months when evaluating all patients, median PFS is almost one year in patients with partial response and a very substantial 7.3 months in patients with stable disease. Here, we provide an update to our previously disclosed safety and tolerability profile at 250 mg daily, now with 84 patients and more than six months median follow-up. Drug-related adverse events are uncommon, most occurring in fewer than 10% of patients, and most of those being grade I. No related grade IV or V events have been reported. GI events were infrequent and low grade, and there is no rash signal. Importantly, only 8% of patients at 250 mg required dose reduction to 200 mg. None required further dose reduction, and no patient has discontinued for a related adverse event. Those reductions have primarily been for anemia, a well-described on-target effect of PRMT5 inhibition in normal bone marrow cells. This safety profile, including the anemia, has been described by investigators as quote "trivial to manage." Finally, this safety profile suggests that vopimetostat is likely to be readily combinable with either chemotherapy or targeted therapy agents, which we are already seeing in the first cohort of the RAS-on inhibitor combination studies. A total of 64 pancreatic cancer patients have been enrolled. Enrollment was sufficiently robust that earlier this year, we began recruiting only second-line patients in order to provide direct support for our planned pivotal study in this indication. Notably, more than half of the 64 pancreatic cancer patients were treated at the go-forward dose of 250 mg. Here, the Kaplan-Meier analysis is presented, comparing second-line to third-line plus patients. As has been seen in other recent pancreatic cancer data sets, the durability in second-line patients is meaningfully better than third-line plus patients. In the second-line patients with a median follow-up of 7.8 months, the median PFS is 7.2 months, and the overall response rate is 25%, a notable improvement over standard of care. Additionally, the median PFS of 7.2 months exceeds the median overall survival, typically seen with standard-of-care chemotherapy in this setting. To compare vopimetostat to current standard-of-care chemotherapy, our median PFS data are plotted versus historical trial data, demonstrating that vopimetostat more than doubles the median PFS reported in these studies. Of note, the control arm of our upcoming pivotal study may be shifted to the left, as several recent studies have shown that MTAP deletion is a negative prognostic marker associated with inferior overall survival across indications, including in pancreatic cancer. While we will not power the study for this effect, it may increase our likelihood of success because in our control arm, all patients will be MTAP-deleted in contrast to these historical controls. Our proposed study design is straightforward, randomizing patients to vopimetostat or a choice of one of four standard-of-care chemotherapy regimens in second-line MTAP-deleted pancreatic cancer. Allowing both gemabraxane and 5-FU-containing regimens in the control arm ensures that patients may be enrolled regardless of the first-line therapy they receive, and it allows for utilization differences between the U.S., Europe, and other areas of the world. We expect that this trial will enroll quickly, given the experience with our first in-human study and the high unmet need in these patients. This study has generated considerable excitement, and we are proud to be the first to evaluate the promising combination of a PRMT5 inhibitor and RAS inhibitors in both pancreatic and lung cancer. The first dose cohort is complete. Exposures were in the active range for each compound, and both combinations have been well tolerated to date. We are backfilling both combination arms, and investigator enthusiasm is high, driving rapid enrollment. Cohort 2 is enrolling, and we anticipate backfilling this cohort at the completion of the DLT observation period. Once go-forward doses have been determined, we plan to open a cohort of first-line patients to gather data needed to enable a pivotal study in this setting. As RAS inhibitors transform the care of people with pancreatic cancer, these combinations have the potential to support a chemotherapy-free first-line pivotal study with competitive timelines. As noted previously, lung cancer patients can be challenging to enroll in clinical studies in general due to the multiple trial options available. Thus, these data are less mature than pancreatic cancer, with only 12 of 41 patients having reached the six-month follow-up threshold. Emerging data are consistent with expectations, and we will provide an update on this cohort in 2026 as the data mature. The histology-agnostic cohort is a collection of multiple late-line difficult-to-treat cancers, representing approximately 20,000 MTAP-deleted patients per year in the U.S. Many of these patients were enrolled early in the study, providing a substantive number of patients with mature data. The nine sarcoma patients enrolled in the study and included in the overall analysis on slide 8 are excluded from the analysis of this cohort because there is no evidence of vopimetostat activity in this cancer type. The overall response rate was 0%, and they will not be included in any further development plans. In this cohort, the overall response rate is 49%, with a striking median PFS of 9.1 months, an indication of activity not previously reported with this class of drugs. As indicated by the black dots, 21 of these 37 patients are ongoing, a measure of remarkable durability in this group of late-line difficult-to-treat patients. Additionally, as indicated by the color coding in the graph, the activity observed in this cohort was seen across the 13 histologies represented, with no single cancer type driving the overall response rate. In order to evaluate the activity of vopimetostat versus standard-of-care treatments for this diverse group of cancers, we plotted the results of several trials representative of the enrolled cancer types and lines of therapy. As was the case with second-line pancreatic cancer, median PFS is more than double the available treatment options. These data provide further evidence of the robust single-agent activity of vopimetostat and provide us with development optionality beyond pancreatic and lung cancer. In summary, the data we've shown today demonstrate that vopimetostat has the potential to be both best in class and first to market for multiple large patient populations with high unmet medical needs. We are planning our first pivotal study of single-agent vopimetostat in second-line MTAP-deleted pancreatic cancer next year. The ongoing combination study of vopimetostat with daraxonrasib and zoldonrasib, in collaboration with Revolution Medicines, puts vopimetostat in the lead to take advantage of the impact RAS inhibitors will have on standard of care in pancreatic cancer. Finally, the potentially best-in-class safety and tolerability profile of vopimetostat to date suggests that as development advances, vopimetostat will be readily combinable with other agents. I will turn it back to Barbara for closing comments. Thank you, Adam. Before we open to Q&A, I want to say that I believe the data we are presenting today represent a potential turning point for patients with multiple hard-to-treat cancers. As an oncologist, I am tremendously proud of all the work that led up to today and the people who made it happen. In summary, these data provide the basis for a $225 million financing announced this morning, reinforce our assertion that vopimetostat has the potential to be the best in class and first to market MTAP-selective PRMT5 inhibitor, support our strategy to start a pivotal study in second-line pancreatic cancer in 2026, give us the confidence in our plans to move into first-line pancreatic cancer in combination with RAS inhibitors with competitive timelines, and highlight the remarkable single-agent activity of vopimetostat in our histology-agnostic cohort. This provides a potentially important opportunity for these patients in an environment where pursuing individual approvals in each of these indications is not feasible. In closing, I want to thank the many, many people at Tango, our founding scientists and collaborators, and most of all, the patients who put their trust and their lives in our hands in choosing to participate in our first in-human study of vopimetostat. vopimetostat is one of the things I'm most proud of in my long career, which has seen many fundamentally important advances in cancer treatment. I, along with the rest of the Tango team, am committed to realizing its potential for as many patients as possible. Now, we'll take questions. Thank you. Ladies and gentlemen, to ask a question at this time, you will need to press star one one on your telephone and wait for your name to be announced. To withdraw your question, simply press *star one one again. As a reminder, in order to accommodate all participants in the queue, please limit your questions to one question per person. Please stand by while we compile the Q&A roster. Our first question coming from the line of Eric Schmidt with Cantor Fitzgerald. Your line is now open. Thanks for taking my question, and congrats Tango team on a seminal moment for vopimetostat's development and just some remarkable tolerability and activity data. Barbara, it sounds like since we last spoke, you've maybe reached some alignment with your friends at Revolution Medicines on this first-line cohort that is in planning, combining RAS inhibitors with MTAP, sorry, with PRMT5 inhibition. Is it true that that's kind of a new development? What would be the next steps after that cohort? Do we have further alignment on other activities and actions? Thank you. Thanks, and thanks, Eric, for your comments on vopimetostat. There's been no change in our collaboration with Revolution Medicines. I think we've always thought that this was a potential path to first-line therapy in pancreatic cancer, and that hasn't changed. That will, of course, be dependent on emerging data, and we'll look forward to disclosing that for the first time next year. What is sort of rate limiting for starting the pivotal second-line study in 2026? We plan an FDA interaction on that study this year, and we're working on study startup actually now at risk. It's really an operational timeline at this point. Thanks. Congrats again. Thank you. Thank you. Our next question coming from the line of Michael Schmidt with Guggenheim. Your line is now open. Hey, guys. Good morning. Congrats on the update. I have to say I'm a tiny bit confused about some of the patient numbers that are mentioned throughout the slide deck. I just wanted to confirm, the 27% overall response rate across all patients, is that based on 94 patients that were evaluable or 85, which is listed on slide seven? Similarly, how many patients were efficacy evaluable in total in the pancreatic cancer cohort? First of all, thanks, Michael. I appreciate the comments. I'm going to turn it over to Adam to go through the numbers because they are a little bit confusing. Sure. The disconnect you're seeing, Michael, between 85 and 94 comes from the fact that that table was an analysis we did about a month before the final data cut. The 27% is the same, but an additional nine patients or so matured to the following waterfall plot, which was two weeks later. Therefore, there are 94 patients represented on the waterfall plot. The 27% overall response rate is actually the same in both of those. In terms of the total number of evaluable patients in pancreatic cancer, if you turn to the slide which speaks to the patient numbers, there were eight patients in the second line assessable for tumor evaluability. In the later lines, there were many more. I don't remember the exact number. 29 of the 34 patients had reached the six-month threshold of evaluability, and somewhere in the neighborhood of 24 or 25 of them were evaluable for tumor. OK. Great. Thanks. Just a follow-up around the longer-term development strategy. How do you think you are positioned in pancreatic cancer longer term? I know the daraxonrasib combination obviously holds a lot of promise. In the near term, you have Bristol doing a first-line PDAC study with chemotherapy, and you have presumably daraxonrasib on the market prior to your second-line study reading out. How do you think about the evolving landscape in PDAC in that context? Thank you, Michael. It is a complicated space right now, which, of course, is really exciting for patients after such a long period of no further development. In terms of our thinking about our path forward, first of all, as we mentioned, we're going to start the second-line study as soon as possible, which we believe will be valuable both for patients and for the company going forward for patients post-chemotherapy and post-RAS inhibitors until there is a PRMT5 inhibitor in first-line pancreatic cancer. Our plans are that that would be us, both vopimetostat, likely in combination with the RAS inhibitor. In terms of the Bristol study, I can only, of course, comment on what's on clinicaltrials.gov. What is there is a plan for a six-arm dose-finding study scheduled to start later this year and the readout of a pivotal study of gemabraxane plus [BGM0504] that would read out in 2029 or 2030. As I mentioned in our remarks, we believe that RAS inhibitors will change the paradigm of treatment in first-line pancreatic cancer. Therefore, moving forward, as we said, with competitive timelines to the Bristol study, not with a combination of chemotherapy and vopimetostat, but with a RAS inhibitor and vopimetostat. Thank you. Thank you. Thank you. Our next question coming from the line of Maury Raycroft with Jefferies. Your line is now open. Hi. Good morning. I'll add my congrats on the data update, and thanks for taking my questions. I'm wondering if you could talk more about the combo study. How many cohorts do you project you'll need? Can you generally comment on what you're seeing so far in cohort one on efficacy and safety, and how doses could shape up there? Thanks, Maury. In terms of the cohort planning, of course, it's a dose escalation study, so it's difficult for us to comment until we have data from each individual dose cohort moving forward. As the exposure of all three compounds was well within the active range in the first cohort, I don't expect that it will be very many dose escalation cohorts. In terms of additional data or color that we can provide, we're not disclosing any additional information from what's on the slide. Got it. Maybe just a quick follow-up. If you can comment on the 3.5 months median time to response versus Bristol' s 5 months and just what could be driving that. We do believe that vopimetostat has substantively better target coverage at 250 mg than BMX-504 does at 400 mg or 600 mg. It's possible that that is partly what's driving it. It's hard to say for sure with the limited data that we have available to do a comparison of the individual patients. That's certainly a possibility. Got it. OK. Thanks for taking my questions. Thank you. Thank you. Our next question coming from the line of Peter Lawson with Barclays. You line is now open. Great. Thanks so much. Congrats on the encouraging data. Maybe just on the pivotal trial design for the second line, I wonder if you could kind of walk through the final elements that are still under discussion with the FDA, and if there's any debate around control regimens or anything you can talk about specifically for power. I assume OS is going to be the primary endpoint. You're talking about the second-line pancreatic cancer study? Yeah. Yeah. As I briefly just mentioned, we have an FDA interaction scheduled and coming up. Anything I say here is a bit speculative until we've had that meeting. The size of the trial is estimated to be about 300 patients, which should be sufficient to detect the differences that we've described. In terms of the chemotherapy regimens, the selection of them are similar, if not identical, to the design used by Revolution Medicines of the three 5-FU-containing regimens and gemabraxane as options for investigators. It's not a full investigator's choice. It'll be from that menu. That has been acceptable to the FDA, as I mentioned, in the Revolution Medicines study. Thank you. The histology-agnostic responses, really strong response that you saw there. As you think about taking that forward, are there particular indications you would exclude, or have you got a good sense from the FDA what indications you have to include and the number of patients? Yeah. First of all, I just want to remark that our pancreatic cancer development path is our first priority, and we have to remain focused on that. As it's been highlighted a few times, those are very competitive timelines, and it's important for us to move that forward as quickly as possible. Having said that, we also are very excited about the data in the histology-agnostic cohort, but we have not yet had an interaction with the FDA on that. It certainly is as well. The The data, both the overall response rate and the median PFS, are well within the range of multiple histology-agnostic studies that have been approved in the past. Bear in mind, histology-agnostic may not be the best name for this cohort because we're not trying to include all cancers. We're trying to include the cancers that are in this cohort. That means it wouldn't include pancreatic or lung cancer, which are being developed separately. As Adam mentioned, it wouldn't include a request to have sarcoma included in the label because we just don't see any activity in sarcoma. I would briefly mention we do think there's a biologic reason for that, which is MTAP deletion. It's heterogeneous in most sarcomas, therefore likely not a truncal mutation the way it is with all other solid tumors that we're aware of. Perfect. Thank you so much. Thanks for the clarity. Thanks, Peter. Thank you. Our next question coming from the line of Robert Driscoll with Wedbush. Your line is now open. Thanks. Good morning, everyone. Thanks for taking the question, adding to the congratulations here on all the progress and the data. I wanted to ask about the MTAP deletion screening rate for the patients that you've attempted to roll in the study in pancreatic cancer. Is it matching the known prevalence of MTAP deletion? Overall, the estimated incidence of genetic screening for patients in the U.S. is about 40%, but it is not uniform across cancer types, and there's a heavy bias towards lung cancer in that number. Certainly, at the beginning of our studies, getting patients screened for MTAP deletion was a challenge. We don't see that anymore at all as causing any delays in enrolling patients. I think it will, as it has always been in targeted therapies, continue to be a challenge to increase the screening rates in these cancers because that's critical for getting the patients both on studies and later commercially on drugs. Got it. Thank you very much. Thank you. Thank you. Our next question coming from the line of Kelsey Goodwin with Piper Sandler. Your line is now open. Good morning. Thanks for taking my question and congrats on the data. Maybe actually building on testing rates, do you have a sense in front-line PDAC how long it would take from the time of testing to get the results? Would physicians have time to start a targeted therapy, or would they put patients on chemo to wait until the results come? Maybe the dynamics there would be helpful. Thank you. Thanks, Kelsey. It's a great question. What we are moving forward with for companion diagnostics is actually two different assays. Particularly in pancreatic cancer, we're working on a companion diagnostic based on immunohistochemistry screening. I always kind of cringe at that as a geneticist, but in fact, in this setting, immunohistochemistry for MTAP deletion is very clear, black and white. It's a homozygous deletion. It's either there or it's not. That immunohistochemistry staining is something that can be done with 24 or 48-hour turnaround in essentially any hospital in the U.S. and Europe. I think that will facilitate the enrollment of those patients rapidly. In addition to that, we'll be working on an NGS assay with Foundation Medicine that allows the use of that assay as well. People will have the option of either one of those assays. Other than just the uptake and getting physicians to send the test, I don't anticipate any special problems with screening for MTAP deletion as any other genetic alteration for targeted therapy. OK, great. Thank you. Just one follow-up on the phase III. I saw the trial has 300 patients. I know Revolution Medicines is targeting closer to 460, but they have some other hierarchical statistical analyses going on. Maybe just a comment on the delta there and what gives you confidence in 300 patients? Sure. It's actually powered equivalently. The difference is that the Revolution Medicines study has formal coprimary endpoints of PFS and overall survival, which requires them to increase their patients enrolled by about 50% to 450. In contrast, our intent is to pursue a hierarchical design study, which first reads out PFS and then, if and when it is positive, overall survival. Doing it in this fashion does not require spending additional alpha on a coprimary, thus enabling us to enroll fewer patients, which will be faster to accrue. That's great and super helpful, color. Thank you so much for answering my questions and congrats again. Thank you, Kelsey. Thank you. Our next question coming from the line of Yuan Zhi with B. Riley Financial. You line is now open. Thank you for taking our questions and congrats on the data. I was surprised no one is talking about safety here. Maybe, Barbara, you can comment on the safety profile observed so far. What's the DRT here and why not dosing higher than 250 mg here? Thank you. Yeah, thanks. Dosing toxicity in the dose escalation portion of this study was actually bronchocytopenia. That was at 600 mg a day. We then decreased back down to 300 mg a day and explored three dose cohorts: 200 mg, 250 mg, and 300 mg a day. There was a trend towards increasing activity across those doses, but there was a big distinction between 250 mg and 300 mg in terms of the bone marrow suppression. The amount of anemia and thrombocytopenia at 300 mg a day that was seen in those patients, although they felt well and were not symptomatic, about 50% of those patients required a dose reduction because of that. At 250 mg and at 200 mg, that dose reduction rate is 8% and lower. That was the discussion with the FDA, who has agreed that we have satisfied the requirements of Project Optimus with this dose optimization cohort, that the sweet spot between optimized efficacy and really good tolerability was at 250 mg a day. Got it. Maybe a quick follow-up here. In terms of your combination, any overlapping toxicity profile with the PanRAS or GTRP inhibitors that would prevent dosing TNG462 higher at 250 mg? In terms of vopimetostat, we don't have any intention of increasing the dose beyond 250 mg. In fact, the second dose cohort is increasing vopimetostat to 250 mg because we wouldn't expect that it would be more tolerable in combination with the RAS inhibitors than it is as a single agent. We've already determined that 300 mg is a higher dose than we plan to go forward with because of the dose reduction rates. In terms of the RAS inhibitors, both of them are very well tolerated as well, with non-overlapping toxicity in general. As we continue to enroll patients, we're optimistic about the safety and tolerability profile, and we'll be updating you with that in more detail in 2026. Got it. Congrats again. Thank you. Thank you. There are no further questions in the queue at this time. I will now turn the call back over to Dr. Barbara Weber for any closing remarks. Thank you all for your time this morning. If you have any additional questions, please reach out to us directly. This concludes today's conference call. Thank you for your participation, and you may now disconnect.